TRKB, Active Human Recombinant Protein
- Known as:
- TRKB, Active Human Recombinant Protein
- Catalog number:
- 40281
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biotech support group
- Gene target:
- TRKB Active Human Recombinant Protein
Related genes to: TRKB, Active Human Recombinant Protein
- Gene:
- NTRK2 NIH gene
- Name:
- neurotrophic receptor tyrosine kinase 2
- Previous symbol:
- -
- Synonyms:
- TRKB
- Chromosome:
- 9q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2018-07-09
Related products to: TRKB, Active Human Recombinant Protein
Related articles to: TRKB, Active Human Recombinant Protein
- Post-stroke cognitive impairment (PSCI) affects nearly 30% of stroke survivors and substantially limits functional recovery. Brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase-β (Trkβ) signalling plays an important role in synaptic plasticity and cognitive function; however, the contribution of individual NTRK2/Trkβ isoforms to PSCI remains poorly understood. This study investigated (a) isoform-specific NTRK2 mRNA expression, (b) genetic association of the isoform-specific variant rs6559833 with post-stroke cognitive outcomes and (c) DNA methylation patterns potentially regulating NTRK2 expression using blood as primary biosource. Isoform-specific expression was analysed in 50 subjects, rs6559833 was genotyped in 280 ischemic stroke patients, and DNA methylation was assessed in 10 samples using whole-genome bisulfite sequencing. The TRKβ-FL expression was significantly reduced in stroke patients compared with healthy controls, whereas TRKβ-SHC expression was higher in PSCN individuals than in PSCI patients. The latter showed positive correlation with MEK2 expression and memory performance. The 'TT' genotype of the rs6559833 variant showed marginal associations with post-stroke memory status and overall BMSE scores (p = 0.0442 and 0.0488, respectively). Furthermore, hypermethylation was observed within the NTRK2 gene body and in genes encoding its splicing regulators, whereas no evident difference in promoter methylation was observed. Collectively, these findings suggest that Trkβ-SHC expression may be associated with preserved cognitive function after stroke and indicate a potential relationship between isoform-specific NTRK2 expression, genetic regulation and cognitive outcomes in PSCI. - Source: PubMed
Sadhukhan DipanwitaChowdhury RaktimRoy SaranyaRoy ArunimaMaitra ShreyosiGhosh Kartik ChandraMukherjee JoydeepBanerjee Tapas KumarHui Subhra PrakashChakrabarti SaikatBiswas Arindam - Chinese tongue sole (Cynoglossus semilaevis) is a unique model for studying the mechanisms of sex determination and sexual size dimorphism (SSD). Preliminary transcriptome and Weighted Gene Co-expression Network Analysis (WGCNA) analyses have identified the neurotrophic tropomyosin receptor kinase 2 gene (ntrk2), mutations in which lead to disorders such as obesity and developmental delays. To better understand the role of neurotrophic tropomyosin receptor kinase (ntrk) family genes in C. semilaevis SSD, we characterized the ntrk gene family and the ligand of ntrk2, brain-derived neurotrophic factor (bdnf). As a result, six ntrk homologous genes (ntrk1, ntrk2a-w, ntrk2a-z, ntrk2b, ntrk3a, ntrk3b) were identified in C. semilaevis at the genome-wide level. Expression profiling revealed predominant brain and pituitary expression of ntrk2 and ntrk3, with ntrk2a-w exhibiting female-specific patterns in the telencephalon and hypothalamus, and ntrk2a-z/ntrk2b widely expressed in all five brain regions. Six different transcripts for bdnf, the primary ligand for ntrk2, were also characterized. Quantitative RT-PCR further revealed sex-specific expression patterns of bdnf1-6 in the five brain regions. Interaction network prediction showed that ntrk could interact with key molecules related to growth and development including BDNF, NGFa, NGFb, and FGFR. Knockdown of ntrk2 and bdnf in C. semilaevis brain cells significantly reduced the expression of pro-opiomelanocortin (pomc), AMP-activated protein kinase α1 subunit (prkaa1), and leptin receptor (lepr)-genes encoding key components of the leptin-melanocortin energy homeostasis pathway. This suggests that the BDNF/NTRK2 signaling axis may centrally regulate feeding and metabolism in C. semilaevis. Our findings provide molecular and functional clues for exploring the neuroendocrine mechanisms underlying sexual size dimorphism in this flatfish. - Source: PubMed
Publication date: 2026/09/15
Wang ZheZhang YueZhang MinShi YuhongCai ZhenyuXu WentengLi XihongWang Na - Tumor maturation is a property of neuroblastomas but can also be observed in unique cases of primary brain malignancies. We hypothesized that the mechanisms of peripheral and central neurogenic tumor maturation could be similar. This study encompassed 19 cases of neuroblastoma and solitary cases of CNS tumors having undergone a morphologically verified maturation. The tumors were analyzed by sequencing and gene expression profiling. We revealed potential similarity of different tumor types upon maturation, associated with stimulated MAPK, PI3K-AKT-mTOR, and TrkA signaling and suppressed regulation of cell cycle and DNA replication and repair. Tumors completing maturation similarly showed enhanced immunogenicity. The levels of NTRK2 expression increased during maturation. Expression of NTRK1 and positive epigenetic regulators (SWI/SNF subunits) increased prior to maturation and decreased upon the differentiation completion. Expression of negative epigenetic regulators EZH2, HDAC10, HDAC2, and DNMT3A decreased in maturing tumors. These data suggest that central and peripheral neurogenic tumors are likely to have common maturation mechanisms. Molecular scenarios associated with neuroblastoma maturation could be: (1) TrkA signaling (seen in cases presenting in < 18-month-olds), or (2) altered expression of epigenetic regulators and transcription factors (seen in cases presenting in >18-month-olds); treatment-induced maturation of CNS malignancies could involve both scenarios. - Source: PubMed
Publication date: 2026/09/11
Druy Alexander EZverev Ivan AAndreeva Natalia ATarakanova Alexandra VSenchenko Maria AGegeliya Nina VZaytseva Margarita ASanakoeva Agunda VPanferova Agnesa VAbasov Ruslan KUsman Natalia YPetrova Vera SKonovalov Dmitry MRaskin Grigorii ANovichkova Galina AGrachev Nikolay SShamanskaya Tatyana VKachanov Denis YPapusha Ludmila I - Approximately 10% of glioblastomas harbor targetable genomic fusions. participates in a variety of fusion events that drive tumorigenesis. Two previous reports have described fusions in adult glioblastoma patients with poor survival. - Source: PubMed
Publication date: 2026/08/20
Sadanandappa Madhumala KKarbhari NishikaKnowles BrizhaPalisoul Scott MHughes Edward GTafe Laura JZanazzi George JLin Chun-ChiehHong Jennifer - Mesenchymal stem cells (MSCs) possess immunomodulatory and tissuereparative properties and have shown therapeutic potential in acute lung injury (ALI). However, the mechanisms underlying their protective effects remain unclear. This study aimed to evaluate the effects of MSCs on bleomycin-induced ALI and to explore the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/08/24
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